Warfarin exposure and calcification of the arterial system in the rat
Warfarin exposure and calcification of the arterial system in the rat
复制标题
DOI：
10.1046/j.1365-2613.2000.00140.x
复制
发表时间：
2000-02-01
影响因子：
3
通讯作者：
Webster, WS
中科院分区：
文献类型：
--
作者：
Howe, AM;Webster, WS
来自基因敲除小鼠的证据表明，肝外维生素 K 依赖性蛋白（基质 gla 蛋白）对于预防动脉钙化是必需的。本研究的目的是确定大鼠的华法林治疗方案（旨在导致肝外维生素 K 缺乏）是否也会导致动脉钙化。 Sprague-Dawley 大鼠从出生起就接受每日剂量的华法林和维生素 K1 治疗，为期 5-12 周。这种治疗会导致肝外维生素 K 缺乏，但不会影响维生素 K 依赖性凝血因子。治疗结束时，处死大鼠并检查血管系统是否有钙化的证据。所有接受治疗的动物均显示出广泛的动脉钙化。脑动脉、静脉和毛细血管似乎没有受到影响。长期接受华法林治疗的人类可能存在肝外维生素 K 缺乏症，因此他们发生动脉钙化的风险可能会增加。
There is evidence from knock-out mice that the extrahepatic vitamin K-dependent protein, matrix gla protein, is necessary to prevent arterial calcification. The aim of this study was to determine if a warfarin treatment regimen in rats, designed to cause extra-hepatic vitamin K deficiency, would also cause arterial calcification. Sprague-Dawley rats were treated from birth for 5-12 weeks with daily doses of warfarin and concurrent vitamin K1. This treatment causes an extrahepatic vitamin K deficiency without affecting the vitamin K-dependent blood clotting factors. At the end of treatment the rats were killed and the vascular system was examined for evidence of calcification. All treated animals showed extensive arterial calcification. The cerebral arteries and the veins and capillaries did not appear to be affected. It is likely that humans on long-term warfarin treatment have extrahepatic vitamin K deficiency and hence they are potentially at increased risk of developing arterial calcification.